Albumin Reduces Oxidative Stress and Neuronal Apoptosis via the ERK/Nrf2/HO‐1 Pathway after Intracerebral Hemorrhage in Rats

Deng, Shuixiang; Liu, Shengpeng; Jin, Peng; Feng, Sheng-Ya; Tian, Mi; Wei, Pengju; Zhu, Hongda; Tan, Jiaying; Zhao, Feng; Gong, Yi

doi:10.1155/2021/8891373

Cited by 38 publications

(26 citation statements)

References 55 publications

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“…Secondary nerve damage after ICH is mainly due to mitochondria-dependent neuronal apoptosis caused by continuous oxidative stress ( Duan et al, 2016 ), and various antioxidant cellular pathways may become new therapeutic targets to rescue neurons and promote functional nerve restoration during ICH treatment ( Righy et al, 2016 ). In recent years, several studies have demonstrated that curcumin can promote the recovery of neurological function after ICH by inhibiting intracranial oxidative stress and regulating redox balance ( Xie et al, 2020 ; Deng et al, 2021 ). Potent antioxidant drugs can effectively inhibit the rapidly increasing ROS during the early stage of ICH, thereby inhibiting neuronal necrosis ( Zhang et al, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Curcumin Restrains Oxidative Stress of After Intracerebral Hemorrhage in Rat by Activating the Nrf2/HO-1 Pathway

et al. 2022

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Intracerebral hemorrhage (ICH), a severe hemorrhagic stroke, induces cerebral oxidative stress and severe secondary neurological injury. Curcumin was demonstrated to inhibit oxidative stress in the brain after ICH. However, the pharmacological mechanism needs further research. We used an intrastriatal injection of autologous blood to make the rat ICH model, and then the rat was treated with curcumin (100 mg/kg/day). Modified Neurological Severity Score (mNSS) and corner test results showed that curcumin could significantly promote the neurological recovery of ICH rats. Meanwhile, curcumin could substantially reduce ROS and MDA in the tissues around intracranial hematoma and prevent GSH depletion. To explore the pharmacological molecular mechanism of curcumin, we used HAPI cells and primary rat cortical microglia for in vitro experiments. In vitro, heme-treated cells were used as the cell model of ICH to explore the molecular mechanism of inhibiting oxidative stress by curcumin treatment. The results showed that curcumin significantly inhibited heme-induced oxidative stress, decreased intracellular ROS and MDA, and promoted Nrf2 and its downstream antioxidant gene (HO-1, NQO1, and Gpx4) expression. These results suggest that curcumin inhibits oxidative stress by activating the Nrf2/HO-1 pathway. Here, our results indicate that curcumin can promote the inhibition of oxidative stress in microglia by activating the Nrf2/HO-1 pathway and promoting neurological recovery after ICH, providing a new therapeutic target for clinical treatment of ICH.

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Section: Discussionmentioning

confidence: 99%

Curcumin Restrains Oxidative Stress of After Intracerebral Hemorrhage in Rat by Activating the Nrf2/HO-1 Pathway

et al. 2022

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“…Moreover, 3,4-dihydroxyphenylethanol may be a powerful agent in the treatment of EBI after SAH because of its free radical scavenging capacity and modulating the Akt and NF-κB signaling pathway ( Zhong et al, 2016 ; Fu and Hu, 2016 ). In addition to the intervening abovementioned diseases, other drugs commonly used clinically, such as heparin ( Hayman et al, 2017 ), albumin ( Deng et al, 2021 ), and propofol ( Zhang H. B. et al, 2019 ), all projected an antioxidative role. Some authors believe that preconditioning would provide the greatest chance of benefit but is obviously not effective ( Mayor et al, 2013 ; Zolnourian et al, 2019 ; Ruan et al, 2020 ; Otsuka et al, 2021 ).…”

Section: Oxidative Stress In Early Brain Injurymentioning

confidence: 99%

An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage

Lin

Zhao

et al. 2021

Front. Aging Neurosci.

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The main reasons for disability and death in aneurysmal subarachnoid hemorrhage (aSAH) may be early brain injury (EBI) and delayed cerebral ischemia (DCI). Despite studies reporting and progressing when DCI is well-treated clinically, the prognosis is not well-improved. According to the present situation, we regard EBI as the main target of future studies, and one of the key phenotype-oxidative stresses may be called for attention in EBI after laboratory subarachnoid hemorrhage (SAH). We summarized the research progress and updated the literature that has been published about the relationship between experimental and clinical SAH-induced EBI and oxidative stress (OS) in PubMed from January 2016 to June 2021. Many signaling pathways are related to the mechanism of OS in EBI after SAH. Several antioxidative stress drugs were studied and showed a protective response against EBI after SAH. The systematical study of antioxidative stress in EBI after laboratory and clinical SAH may supply us with new therapies about SAH.

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“…OSA aggravates EBI via the ATF4/CHOP signaling pathway following ICH. deng et al (39) reported that the aTF4/cHoP signaling pathway is a key mechanism by which brain injury is ameliorated in icH rats. Therefore, the present study investigated whether OSA aggravated apoptosis and neuroinflammation by regulating the aTF4/cHoP signaling pathway.…”

Section: Osa Further Increases Expression Levels Of Apoptosisassociated Proteins Following Ichmentioning

confidence: 99%

Intermittent hypoxia mimicking obstructive sleep apnea aggravates early brain injury following ICH via neuroinflammation and apoptosis

et al. 2021

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Spontaneous intracerebral hemorrhage (ICH) is a subtype of stroke associated with high mortality and morbidity due to the lack of effective therapy. Obstructive sleep apnea (OSA) has been reported to aggravate early brain injury (EBI) and worsen the overall outcome of patients with ICH. However, the precise role of OSA-mediated neuroinflammation and apoptosis following ICH has not been confirmed. The present study aimed to investigate the neuronal damage induced by OSA and the potential molecular mechanisms by which ICH-induced EBI regulates neural apoptosis in a C57BL/6 mouse ICH model. Mortality, neurological score, brain water content and neuronal death were evaluated by Evans blue extravasation, TUNEL staining, ELISA, analysis of reactive oxygen species/lipid peroxidation and western blotting. The results showed that OSA induction decreased survival rate, neurological score and neuron survival and upregulated the protein expression levels of Caspase-3, Bax, cytokines IL-1β, IL-6 and TNF-α and NF-κB, which indicated that OSA-mediated induction of apoptosis and neuroinflammation aggravated neuronal death following ICH. The molecular mechanism was partly dependent on the activating transcription factor/CHOP pathway. Taken together, the results demonstrated that OSA worsens neurological outcomes in mice and increases neuronal death by enhancing neural apoptosis and neuroinflammation.

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Albumin Reduces Oxidative Stress and Neuronal Apoptosis via the ERK/Nrf2/HO‐1 Pathway after Intracerebral Hemorrhage in Rats

Cited by 38 publications

References 55 publications

Curcumin Restrains Oxidative Stress of After Intracerebral Hemorrhage in Rat by Activating the Nrf2/HO-1 Pathway

Curcumin Restrains Oxidative Stress of After Intracerebral Hemorrhage in Rat by Activating the Nrf2/HO-1 Pathway

An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage

Intermittent hypoxia mimicking obstructive sleep apnea aggravates early brain injury following ICH via neuroinflammation and apoptosis

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